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genderqueerdykes · 1 year ago

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Feminizing HRT Overview, Guide & Information for All People Seeking It

we also have a version of this post for testosterone/masculinizing HRT as well. we wanted to write a companion piece as many folks have asked about this. it has take a bit of time, but here we are!

The testosterone HRT post is here.

Getting Your Prescription

To start taking estrogen, you will need to find a general practitioner, family doctor, endocrinologist or informed consent clinic where you can discuss gender affirming care with knowledgeable staff. Planned Parenthood is a good option for many trans people in general. Your mental health may also be evaluated, and your heart health and screening for a few other health conditions, as well as having access to your family health history if possible will be required.

Check to see if you have medical insurance, either through your family, your job, or if you are low income, a program like medicaid. Search for low income insurance plans in your area if it is needed, many places offer insurance plans for those who can't afford care on their own.

Here is a map of informed consent HRT clinics in the US.

You will discuss any gender dysphoria, gender presentation needs, if you have a support network, how you are impacted by your gender in your every day life with your provider and so on before being given a prescription. You will only be given a prescription after you discuss the risks of HRT and are screened for possible health problems and diseases or ways your body could react negatively to HRT. If you have needle trauma or phobias and can't inject hormones, it's best to bring it up before you get your prescription to save time and confusion.

The Medications

Treatment typically starts with spironolactone (aldactone), an anti-androgen that blocks androgen receptors ("male" sex hormones) for a few weeks, and then add estrogen, but many folks start with spiro and estrogen at the same time. Spiro will lower the amount of testosterone your body makes. For some people, spiro isn't necessary at all!

Some forms of spironolactone are reported to make folks pee like crazy, others do not have as bad of a time with it. Your mileage will vary depending on manufacturer. Spironolactone is intended to be a blood pressure medication, meaning it is a diuretic and is intended to help your body flush out fluids + salt. You will need to keep yourself hydrated if you notice this effect, as well as increasing electrolyte intake where possible.

Estrogen also lowers how much testosterone your body makes, and triggers changes in the body that occur during puberty in afab & adjacent people. Estrogen can be taken several ways, and is usually taken daily, and several times a day. You can take it in a pill or shot, and several forms of estrogen that can be applied to the skin like creams, gels and patches.

Make sure you thoroughly sanitize the skin of any injection sites or areas you will be applying gel or patches. If you are given topical estrogen, make sure you wash your hands after application and do not have someone else apply it for you. Make sure you do not go swimming or shower within several hours of application to make sure your skin absorbs the hormone.

You may not need to take anti androgens if you are doing estrogen injections, depending on how effective the estrogen injections are for you. Some people may not end up needing anti-androgens at all, and may be able to skip that entirely as spiro has unwanted side effects. Your natural hormone levels will dictate whether or not it's necessary, but it is not necessary for everyone.

You may end up being recommended to switch from one form of estrogen to another as your transition progresses, depending on how your body responds.

It's recommended to not take estrogen as a pill if you have personal/family history of blood clots in a deep vein or in lungs (venous thrombosis).

Some people also end up taking progesterone as well alongside estrogen. Progesterone is typically taken to encourage breast tissue growth, as this is the most prominent effect of the hormone. If sufficient breast tissue growth isn't seen from estrogen alone, progesterone can be added to your regimen, though this is only done later on into treatment, around a year or so in.

If you choose injectable estrogen, make sure to listen to your provider and ask for instructions about how to use needles and syringes, as well as injection angles, how and where you'll be injecting. Do not inject in the exact same spot every time, this can prevent the issue from healing properly and create scar tissue or cause infections or skin tissue necrosis (death). You also need a sharps container to safely dispose of your needle tips. Never re-use a needle, even if it was used previously on yourself. Always ask the pharmacy if you need more needles. A lot of places let you get them in bulk.

If you are going the injection route, make sure you know whether or not you are instructed to do intramuscular or subcutaneous injections. Intramuscular injections usually taper out of the system more quickly and need to be done more frequently, where as many patients find subcutaneous injections less painful and easier as they can be done less frequently.

For more information on safe intramuscular or subcutaneous injection for estrogen, please read here.

Another option for feminizing HRT is to take gonadotropin-releasing hormone (Gn-RH) analogs. They lower the amount of testosterone your body makes and may allow you to take lower doses of estrogen without using Spiro. Gn-RH analogs are usually more expensive, but are an option if for whatever reason the conventional route can't work for you.

DON'T GIVE UP IF YOU DON'T SEE THE EFFECTS YOU WANT TO SEE RIGHT AWAY! Many of them can take a long time to develop, often times patience is the key. If you wait it out and still don't see the results you'd like, you can try another route. Don't give up, a lot of people get deterred in the early stage of transition, you'll get there with patience and communication.

Stay patient, stay positive!

What to Expect from Feminizing HRT

Less facial and body hair growth: typically happens 6 - 12 months after treatment starts. Full effects within ~3 years on average.

Slower scalp hair loss: begins 1 - 3 moths after treatment begins. Full effect between 1 - 2 years on average.

Softer, less oily skin, and changes in general skin texture: 3 - 6 months after treatment starts, full effects within 2 - 3 years on average

Rounder, softer features including face and body, and more body fat: 3 - 6 months after treatment starts, full effects in 2 - 5 years.

Breast development: begins 3 - 6 months after treatment starts, full effects within 2 - 5 years on average or more, according to medical studies, but it can vary wildly from person to person, give dosage and hormones taken. If desired effects are not seen, progesterone can be taken alongside estrogen to help after around one year on estrogen. When breast growth begins, it starts with hard lumps under the nipples along with some soreness and itchiness. Some have sore breasts for a long time, and some may get scared and think they have cancer during this stage. Breasts will be swollen and tender for good while, and nipples may be especially sensitive to even light touch.

Reduced muscle mass/density: 3 - 6 months after treatment starts, full effect in 1 - 2 years on average

Potential decrease in libido if on estrogen alone, though not guaranteed: If it happens, it's generally within 1 - 3 months in and can last a while, but may even out over time

Fewer erections, decreased ejaculate volume, and erections that can become painful or uncomfortable if frequent erections are not maintained. This begins 1 - 3 months after treatment starts, and the full effect is within 3 - 6 months. Regularly maintaining erections and frequent ejaculation can ease some of these uncomfortable feelings in some people.

Changes in how orgasms feel, changes in texture and degree of sensation of penis and scrotum skin as well as changes in body odor: typically begins within 3 - 6 months, though it varies from person to person. Often times the way one's body responds to orgasms completely changes, many people find themselves experiencing full-body orgasms and more intense erogenous zones elsewhere in the body other than the genitals.

Smaller testicles, or testicular atrophy happens within 3 - 6 months and the full effects are usually seen within 2 - 3 years.

Increase in size of bladder and decrease in size of prostate over time which can lead to making one's gspot harder to find, and make prostate examinations more difficult, though they are still vital, as prostate cancer is still a possible factor.

Potential mood fluctuations while adjusting to the hormones, many report increased crying and sadness during the first 3 - 6 months with this tapering off after a full year at most.

Increased fatigue while adjusting to the hormones, sleepiness and becoming easily exhausted are common reports. This can vary drastically from person to person, ymmv.

If you have testicles and choose to have them removed, you may need to take testosterone as well as estrogen in order to have a healthy endocrine system. You will need to discuss the effects of this with your specialists if you want to go this route. If your androgen levels get too low because your body cannot synthesize enough testosterone after bottom surgery, you may need additional medication.

Potential infertility, though this is not a guarantee, and safe sex should still be practiced at all times. No timeline projected though the longer one is on E the more likely it becomes.

Monthly cycles akin to menstrual cycles: these are not present in everyone, but many people report entering a cycle of extreme fatigue, body aches, abdominal cramping in the approximate area where a uterus would sit, headaches, and more for around the duration of a menstrual cycle (4 - 10 days on average).

Progesterone inversely to estrogen can cause an increase in libido in most who take it, and is the primary hormone used for breast growth. Lactation may also occur while taking prog, if this happens, talk to your doctor right away.

Keep track of your progress when and where you are able, and don't be afraid to bring up any concerns you may have with your professionals or trans friends, or any other trans resource. Your transition is in your hands and you're allowed to modify it as you see fit. If you do not see the effects you want from traditional HRT, you may be able to seek the Gn-RH route, and if you aren't seeing the results you want from just estrogen, progesterone might be of use to you.

You will need to keep an eye on your bone health as high levels of estrogens can increase your chance to develop osteoporosis, and potential new cancers like breast cancer may arise, as well as heart problems. Getting checkups as frequently as possible and communicating with your doctor/s will be of great use when and where possible

Either way, we hope this helps in some way! We will add to it as we find/think of more information. Good luck to everyone seeking feminizing HRT, you deserve to look and feel like yourselves!

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covid-safer-hotties · 4 months ago

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The Long-term Complications of Covid-19 Infection - Published Sept 13, 2024

Context.— As the Covid-19 pandemic continues into its 4th year, reports of long-term morbidity and mortality are now attracting attention. Recent studies suggest that Covid-19 survivors are at increased risk of common illnesses, such as myocardial infarction, diabetes mellitus and autoimmune disorders. Mortality may also be increased. This article will review the evidence that supports some of these observations and provide an opinion about their validity and their relevance to insured cohorts.

Background Many Covid-19 survivors report protracted symptoms, sometimes lasting 3 years or more. These are collectively called post-acute sequelae of SARS-CoV-2 infection (PASC) or long Covid. They have been frequently described.1–4 In the past year, reports of long-term complications such as atrial fibrillation, heart failure, stroke and pulmonary embolism have emerged. In some reports these established disease entities are erroneously described as long Covid, generating confusion. The distinction is important: illness reported in Covid survivors are not restricted to the long Covid cohort. Thus, they are relevant to the majority of the North American population who have been infected by SARS-CoV-2, and not just the estimated 5-10% of individuals who belong to the long Covid cohort. This paper will examine the reports of increased incidence of cardiovascular diseases in both and will examine the reported long-term increase in mortality.

Cardiovascular disease after 1 and 2 years Multiple studies have reported an increased risk of cardiovascular events at 1 year. A February 2022 analysis of 153,760 US veterans, followed for 1 year after Covid-19 infection, reported an increased risk of cerebrovascular disease (HR 1.53), ischemic heart disease (HR 1.66), thromboembolic disease (HR 2.39) and atrial fibrillation (HR 1.71).5 Risk was greatest in those hospitalized and those with pre-morbid illnesses. However, risk was also elevated in outpatients, who constituted the vast majority of the cohort. These findings have been corroborated in 2 further studies. In a 2023 analysis of 690,000 Covid-19 survivors, drawn from the TriNetX database–self-described as the world’s largest global Covid-19 dataset–there was an increased risk of cerebrovascular disease (HR 1.6), ischemic heart disease (HR 2.8), thromboembolic disease (HR 2.6) and atrial fibrillation (HR 2.4) at 1 year.6 In contrast to the VA study which examined a predominantly older male population, the subjects in this study were younger, with mean age 44, and 57% were female. Risk was higher in the >65 age group and was not limited to inpatients. In a May 2023 Lancet retrospective analysis of 535,000 Hong Kong (HK) and 16,000 UK Covid 19 survivors, similar hazard ratios were recorded for stroke (HR 1.2), ischemic heart disease (HR 1.32), atrial fibrillation (HR 1.31) and deep venous thrombosis (HR 1.74).7 However, it is worth noting that while follow-up was described as 28 months for the HK cohort and 17 months for the UK cohort, the median follow-up for the HK group was 146 days and was 243 days for the UK cohort, somewhat limiting the conclusions of true impact at 1 year. Contradicting these studies, a prospective analysis of 17,000 Covid-19 survivors in the UK Biobank, did not document an increased risk of cardiovascular outcomes amongst outpatients, with the exception of thromboembolic disease (HR 2.7).8 An August 2023 analysis of 138,000 VA Covid-19 survivors followed for 2 years– the longest follow-up period to date– reported that the risk of complications in outpatients had returned to baseline at 6 months.9 In contrast, the risk for multiple cardiovascular and thromboembolic complications in the hospitalized cohort remained elevated at 2 years. None of these 5 studies was limited to individuals with long Covid, but similar findings have been reported in this group: a recent analysis of 13,435 individuals who had been diagnosed with long Covid, based on a typical array of symptoms, reported increased risks at 1 year for ischemic heart disease (HR 1.7), ischemic stroke (HR 2.1) and pulmonary embolism (HR 3.6).10

These studies document a fairly consistent, increased risk of cardiovascular complications among Covid-19 survivors. However, important questions remain. Amongst these: does increasing population immunity and vaccination change the risk? Is the magnitude of risk similar for all SARS CoV-2 variants? Does reinfection increase the risk? Answers to some are available. Vaccination appears to attenuate the risk: a Korean study of 592,000 individuals post-Covid-19 infection, showed that vaccination decreased the risk of heart attack and stroke by approximately 50%.11 This finding was replicated in a large US cohort where major adverse cardiovascular events were reduced by a similar amount for full vaccination, and by 25% for partial vaccination.12 Thus, while vaccination does not eliminate long-term complications, it appears to provide a substantial protective effect.

Reinfection may increase the risk of sequelae. In a large US VA cohort of 440,000 Covid survivors, of whom 40,000 had one or more SARS-CoV-2 reinfections, the risk of cardiovascular disorders was increased (HR 3.02), when compared to a single infection.13 Moreover, this risk was not modified by vaccination.

The impact of different variants is less clear. Most of the described studies were conducted in 2020-2021 when delta and pre-delta variants predominated. It is unclear whether similar outcomes would characterize infection with Omicron variants, which remain dominant in most countries since November 2021. Interestingly, the risk of cardiovascular complications in the cohort of Hong Kong survivors described above, where the Omicron was the prevalent strain, was no different than among the comparator UK Biobank cohort, where pre-Omicron strains were prevalent.7

Is there extra long-term mortality after Covid-19 infection? Extra mortality has been reported by several studies.6,8,14–18 A 2021 US analysis of 400 Covid-19 survivors, documented increased mortality (HR 2.5) at 1 year.14 The additional risk was confined to individuals who had been hospitalized. In 2022, 3 studies reported excess mortality in 3 different countries. The first, an Estonian whole-population study of 66,000 Covid-19 survivors, of whom 8% were hospitalized, reported a 3-fold increase in mortality at 12 months.15 Mortality was particularly elevated in the first 5 weeks following infection. For those over age 60, increased mortality persisted until 12 months (HR 2.8). However, for those less than age 60, mortality was not increased after 35 days. The second, an analysis of 690,000 Covid-19 survivors from the TriNetX database also reported increased 1-year mortality risk (HR 1.6).6 This was largely explained by excess deaths in individuals over age 65; below age 45 risk was not increased. For the outpatient cohort the risk of mortality was lower than that of the comparison group (HR 0.46). The third, a study of 25,000 Covid-19 survivors drawn from the UK Biobank, reported increased mortality risk at 20 months, for those with severe Covid infection (HR 14.7), but also an increased risk for those with mild disease (HR 1.23).16 Stratification by age was not provided.

In 2023 4 further studies reported similar, but at times quantitatively different results. Two analyses drew on the UK Biobank cohort. In the first, a prospective evaluation of 7,800 SARS-CoV-2 PCR positive individuals, increased mortality was reported for the study group at 18 months (HR 5.0), when compared to both a contemporary and an historical cohort.17 For the non-severe cases the mortality risk remained elevated (HR 4.8). The second study, already described above– a comparative analysis of 7600 Covid survivors from the UK Biobank and 530,000 Covid survivors in Hong Kong–reported increased mortality (HR 4.16) after 17 months for the former and 28 months for the latter.7 The risk of mortality was higher in the UK than the HK cohort, a difference the authors posited was due to Omicron being the dominant variant in HK during the study period. The risk remained elevated, but less so, for younger cohorts and for mild Covid-19 infections.

Finally, 2 large US studies recently reported mortality at 2 years. In the first, an analysis of 138,000 US veteran Covid-19 survivors with 5.9 million controls, the risk of death for the hospitalized cohort remained elevated at 2 years (HR 1.29).8 In contrast, the risk of death for the outpatient cohort returned to baseline at 6 months. Breakdown of risk by age-group was not provided. The second study, also of US veterans, reported similar findings. In a cohort of 280,000 Covid-19 survivors the risk of death remained elevated at 2 years (HR 2.0).18 The risk was highest in the first 90 days (HR 6.3) and decreased at 6 months (HR 1.18). Thereafter, the risk in Covid-19 survivors was slightly less than the control group (HR 0.89). A post-hoc subgroup analysis examined and refuted the possibility that accelerated mortality in the control group could have explained the lower mortality in Covid-19 survivors. The risk of death in hospitalized individuals remained elevated at 2 years (HR 1.22).

How Plausible is this Information? The studies described above command attention by virtue of their size and the consistency of their findings in different populations, and in different countries. They are also supported by the observations of long-term pathophysiologic abnormalities following SARS-CoV-2 infection, such as ongoing inflammation, persistence of virus, and immune system dysfunction. However, the negative ledger is also substantial. Observational studies such as these, no matter how well-designed, remain open to many types of bias. Reliance on diagnostic codes, prescription records, laboratory results and tallies of clinical visits, to establish disease incidence, is intrinsically error-prone and makes cross-study comparisons difficult. Perhaps more importantly, the cohorts described above were different in many respects, varying from the older, male-predominant cohort of the US VA system to the younger healthier cohort of the UK Biobank. Further, cohorts were constituted during the first year of the pandemic, at a time when healthcare delivery was disrupted, lockdowns were in effect, vaccination and antivirals were largely unavailable, and population immunity levels were low. Thus, it could be argued that the observed outcomes are better explained by an evolving pandemic, rather than solely SARS-CoV-2 infection. This could also explain the most recent reports that after 2 years of follow-up, the risk of both Covid-19 complications and mortality, in most of those infected (i.e., the non-hospitalized), is no longer elevated. It also evident that most of the reported extra mortality is occurring in the early months following infection, where survival curves separate rapidly.6,10,15,18

Are these findings relevant to an insured population? ‘Partially’ is probably the best answer. The most important observation is that hospitalization, and in-particular an intensive care unit admission, is the dominant risk factor for both morbidity and mortality. This risk appears to persist up to 2 years. The second important risk element is the presence of comorbid conditions. This observation raises the interesting question of what exactly causes the extra mortality. Is it due to ‘protracted’ SARS-Co-V-2 infection or is it caused by a recognized complication of Covid-19, such as pulmonary fibrosis or acute kidney injury? Or is it explained by an aggravation of a comorbid illness? Or is it a complication of long Covid? There is a likelihood that all these mechanisms were at play in the cohorts under study.

For non-hospitalized individuals, and those that are healthy, the evidence for extra morbidity and mortality after the first 3-6 months is far from conclusive. For the long Covid cohort, the evidence for additional mortality requires further supporting evidence. As the prevalence of co-morbid conditions is lower in insured populations, one might reasonably expect, based on current evidence, that longer-term morbidity and mortality due to Covid-19 infection will be minimally affected.

References 1.Davis H, McCorkell L, Vogel, J. et al Long COVID: major findings, mechanisms and recommendations. Nat Rev Microbiol 21, 133–146 (2023). doi.org/10.1038/s41579-022-00846-2

2.Meagher T. Long COVID - An Early Perspective. J Insur Med. 2021 Jan 1;49(1):19–23. doi: 10.17849/insm-49-1-1-5.1. PMID: 33784738.

3.Meagher T. Long COVID – One year On. J Insur Med. 2022 Jan 1;49:1–6. doi: 10.17849/insm-49-3-1-6.1. PMID: 33561352.

4.Meagher T. Long Covid - Into the Third Year. J Insur Med 2023;50(1):54–58. doi.org/10.17849/insm-50-1-54-58.1

5.Xie Y, Xu E, Bowe B et al Long-term cardiovascular outcomes of COVID-19. Nat Med 28, 583–590 (2022). doi.org/10.1038/s41591-022-01689-3

6.Wang W, Wang CY, Wang SI et al Long-term cardiovascular outcomes in COVID-19 survivors among non-vaccinated population: A retrospective cohort study from the TriNetX US collaborative networks. eClinicalMedicine. 2022 Nov;53:101619. doi: 10.1016/j.eclinm.2022.101619

7.Lam I, Wong C, Zhang, R et al Long-term post-acute sequelae of COVID-19 infection: a retrospective, multi-database cohort study in Hong Kong and the UK. eClinicalMedicine Vol. 60 Published: May 11, 2023. doi: doi.org/10.1016/j.eclinm.2023.102000

8.Raisi-Estabragh Z, Cooper J, Salih A, et al Cardiovascular disease and mortality sequelae of COVID-19 in the UK Biobank Heart 2023;109:119–126.

9.Bowe, B., Xie, Y. & Al-Aly, Z. Postacute sequelae of COVID-19 at 2 years. Nat Med 29, 2347–2357 (2023). doi.org/10.1038/s41591-023-02521-2

10.DeVries A, Shambhu S, Sloop S et al One-Year Adverse Outcomes Among US Adults With Post–COVID-19 Condition vs Those Without COVID-19 in a Large Commercial Insurance Database. JAMA Health Forum. 2023;4(3):e230010. doi:10.1001/jamahealthforum.2023.0010

11.Kim Y, Huh K, Park Y et al Association Between Vaccination and Acute Myocardial Infarction and Ischemic Stroke After COVID-19 Infection. JAMA. 2022;328(9):887–889. doi:10.1001/jama.2022.12992

12.Jiang J, Chan L, Kauffman J, et al Impact of Vaccination on Major Adverse Cardiovascular Events in Patients With COVID-19 Infection. J Am Coll Cardiol. 2023 Mar, 81(9):928–930. doi.org/10.1016/j.jacc.2022.12.006

13.Bowe B, Xie, Y, Al-Aly Z. Acute and postacute sequelae associated with SARS-CoV-2 reinfection. Nat Med 28, 2398–2405 (2022). doi.org/10.1038/s41591-022-02051-3

14.Mainous AG, Rooks BJ, Wu, et al COVID-19 post-acute sequelae among adults: 12 month mortality risk. Front Med (Lausanne). 2021;8:778434. doi:10.3389/fmed.2021.778434

15.Uuskula A, Jurgenson T, Pisarev H et al Long-term mortality following SARS-CoV-2 infection: A national cohort study from Estonia. The Lancet Regional Health - Europe 2022;18:100394 Published online 29 April 2022. doi.org/10.1016/j.lanepe.2022.100394

16.Xiang Y, Zhang R, Qiu G. et al Association of Covid-19 with risks of hospitalization and mortality from other disorders post-infection: A study of the UK Biobank. medRxiv doi: doi.org/10.1101/2022.03.23.22272811

17.Wan E, Mathur S, Zhang R et al Association of COVID-19 with short- and long-term risk of cardiovascular disease and mortality: a prospective cohort in UK Biobank, Cardiovascular Research, Volume 119, Issue 8, June 2023, 1718–1727. doi.org/10.1093/cvr/cvac195

18.Iwashyna TJ, Seelye S, Berkowitz TS, et al Late Mortality After COVID-19 Infection Among US Veterans vs Risk-Matched Comparators: A 2-Year Cohort Analysis. JAMA Intern Med. Published online August 21, 2023. doi:10.1001/jamainternmed.2023.3587

#mask up #covid #pandemic #covid 19 #wear a mask #public health #coronavirus #sars cov 2 #still coviding #wear a respirator

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myrawjcsmicasereports · 3 months ago

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Retinal and choroidal vascular drop out in a case of severe phenotype of Flammer Syndrome. Rescue of the ischemic-preconditioning mimicking action of endogenous Erythropoietin (EPO) by off-label intra vitreal injection of recombinant human EPO (rhEPO) by Claude Boscher in Journal of Clinical Case Reports Medical Images and Health Sciences

Abstract

Background: Erythropoietin (EPO) is a pleiotropic anti-apoptotic, neurotrophic, anti-inflammatory, and pro-angiogenic endogenous agent, in addition to its effect on erythropoiesis. Exogenous EPO is currently used notably in human spinal cord trauma, and pilot studies in ocular diseases have been reported. Its action has been shown in all (neurons, glia, retinal pigment epithelium, and endothelial) retinal cells. Patients affected by the Flammer Syndrome (FS) (secondary to Endothelin (ET)-related endothelial dysfunction) are exposed to ischemic accidents in the microcirculation, notably the retina and optic nerve.

Case Presentation: A 54 years old female patient with a diagnosis of venous occlusion OR since three weeks presented on March 3, 2019. A severe Flammer phenotype and underlying non arteritic ischemic optic neuropathy; retinal and choroidal drop-out were obviated. Investigation and follow-up were performed for 36 months with Retinal Multimodal Imaging (Visual field, SD-OCT, OCT- Angiography, Indo Cyanin Green Cine-Video Angiography). Recombinant human EPO (rhEPO)(EPREX®)(2000 units, 0.05 cc) off-label intravitreal injection was performed twice at one month interval. Visual acuity rapidly improved from 20/200 to 20/63 with disparition of the initial altitudinal scotoma after the first rhEPO injection, to 20/40 after the second injection, and gradually up to 20/32, by month 5 to month 36. Secondary cystoid macular edema developed ten days after the first injection, that was not treated via anti-VEGF therapy, and resolved after the second rhEPO injection. PR1 layer integrity, as well as protective macular gliosis were fully restored. Some level of ischemia persisted in the deep capillary plexus and at the optic disc.

Conclusion: Patients with FS are submitted to chronic ischemia and paroxystic ischemia/reperfusion injury that drive survival physiological adaptations via the hypoxic-preconditioning mimicking effect of endogenous EPO, that becomes overwhelmed in case of acute hypoxic stress threshold above resilience limits. Intra vitreal exogenous rhEPO injection restores retinal hypoxic-preconditioning adaptation capacity, provided it is timely administrated. Intra vitreal rhEPO might be beneficial in other retinal diseases of ischemic and inflammatory nature.

Key words : Erythropoietin, retinal vein occlusion, anterior ischemic optic neuropathy, Flammer syndrome, Primary Vascular Dysfunction, anti-VEGF therapy, Endothelin, microcirculation, off-label therapy.

Introduction

Retinal Venous Occlusion (RVO) treatment still carries insufficiencies and contradictions (1) due to the incomplete deciphering of the pathophysiology and of its complex multifactorial nature, with overlooking of factors other than VEGF up-regulation, notably the roles of retinal venous tone and Endothelin-1 (ET) (2-5), and of endothelial caspase-9 activation (6). Flammer Syndrome (FS)( (Primary Vascular Dysfunction) is related to a non atherosclerotic ET-related endothelial dysfunction in a context of frequent hypotension and increased oxidative stress (OS), that alienates organs perfusion, with notably changeable functional altered regulation of blood flow (7-9), but the pathophysiology remains uncompletely elucidated (8). FS is more frequent in females, and does not seem to be expressed among outdoors workers, implying an influence of sex hormons and light (7)(9). ET is the most potent pro-proliferative, pro-fibrotic, pro-oxidative and pro-inflammatory vasoconstrictor, currently considered involved in many diseases other than cardio-vascular ones, and is notably an inducer of neuronal apoptosis (10). It is produced by endothelial (EC), smooth vascular muscles (SVMC) and kidney medullar cells, and binds the surface Receptors ET-A on SVMC and ET-B on EC, in an autocrine and paracrine fashion. Schematically, binding on SVMC Receptors (i.e. through local diffusion in fenestrated capillaries or dysfunctioning EC) and on EC ones (i.e. by circulating ET) induce respectively arterial and venous vasoconstriction, and vasodilation, the latter via Nitrite oxide (NO) synthesis. ET production is stimulated notably by Angiotensin 2, insulin, cortisol, hypoxia, and antagonized by endothelial gaseous NO, itself induced by flow shear stress. Schematically but not exclusively, vascular tone is maintained by a complex regulation of ET-NO balance (8) (10-11). Both decrease of NO and increase of ET production are both a cause and consequence of inflammation, OS and endothelial dysfunction, that accordingly favour vasoconstriction; in addition ET competes for L-arginine substrate with NO synthase, thereby reducing NO bioavailability, a mechanism obviated notably in carotid plaques and amaurosis fugax (reviewed in 11).

Severe FS phenotypes are rare. Within the eye, circulating ET reaches retinal VSMC in case of Blood-Retinal-Barrier (BRB) rupture and diffuses freely via the fenestrated choroidal circulation, notably around the optic nerve (ON) head behind the lamina cribrosa, and may induce all pathologies related to acute ocular blood flow decrease (2-3)(5)(7-9). We previously reported two severe cases with rapid onset of monocular cecity and low vision, of respectively RVO in altitude and non arteritic ischemic optic neuropathy (NAION) (Boscher et al, Société Francaise d'Ophtalmologie and Retina Society, 2015 annual meetings).

Exogenous Recombinant human EPO (rhEPO) has been shown effective in humans for spinal cord injury (12), neurodegenerative and chronic kidney diseases (CKD) (reviewed in 13). Endogenous EPO is released physiologically in the circulation by the kidney and liver; it may be secreted in addition by all cells in response to hypoxic stress, and it is the prevailing pathway induced via genes up-regulation by the transcription factor Hypoxia Inducible Factor 1 alpha, among angiogenesis (VEGF pathway), vasomotor regulation (inducible NO synthase), antioxidation, and energy metabolism (14). EPO Receptor signaling induces cell proliferation, survival and differentiation (reviewed in 13), and targets multiple non hematopoietic pathways as well as the long-known effect on erythropoiesis (reviewed in 15). Of particular interest here, are its synergistic anti-inflammatory, neural antiapoptotic (16) pro-survival and pro-regenerative (17) actions upon hypoxic injury, that were long-suggested to be also indirect, via blockade of ET release by astrocytes, and assimilated to ET-A blockers action (18). Quite interestingly, endogenous EPO’s pleiotropic effects were long-summarized (back to 2002), as “mimicking hypoxic-preconditioning” by Dawson (19), a concept applied to the retina (20). EPO Receptors are present in all retinal cells and their rescue activation targets all retinal cells, i.e. retinal EC, neurons (photoreceptors (PR), ganglion (RGG) and bipolar cells), retinal pigment epithelium (RPE) osmotic function through restoration of the BRB, and glial cells (reviewed in 21), and the optic nerve (reviewed in 22). RhEPO has been tested experimentally in animal models of glaucoma, retinal ischemia-reperfusion (I/R) and light phototoxicity, via multiple routes (systemic, subconjunctival, retrobulbar and intravitreal injection (IVI) (reviewed in 23), and used successfully via IVI in human pilot studies, notably first in diabetic macular edema (24) (reviewed in 25 and 26). It failed to improve neuroprotection in association to corticosteroids in optic neuritis, likely for bias reasons (reviewed in 22). Of specific relation to the current case, it has been reported in NAION (27) (reviewed in 28) and traumatic ON injury (29 Rashad), and in one case of acute severe central RVO (CRVO) (Luscan and Roche, Société Francaise d’Ophtalmologie 2017 annual meeting). In addition EPO RPE gene therapy was recently suggested to prevent retinal degeneration induced by OS in a rodent model of dry Age Macular Degeneration (AMD) (30).

Case Report Presentation

This 54 years female patient was first visited on March 2019 4th, seeking for second opinion for ongoing vision deterioration OR on a daily basis, since around 3 weeks. Sub-central RVO (CRVO) OR had been diagnosed on February 27th; available SD-OCT macular volume was increased with epiretinal marked hyperreflectivity, one available Fluorescein angiography picture showed a non-filled superior CRVO, and a vast central ischemia involving the macular and paraoptic territories. Of note there was ON edema with a para-papillary hemorrage nasal to the disc on the available colour fundus picture.

At presentation on March 4, Best Corrected Visual Acuity (BCVA) was reduced at 20/100 OR (20/25 OS). The patient described periods of acutely excruciating retro-orbital pain in the OR. Intraocular pressure was normal, at 12 OR and 18 OS (pachymetry was at 490 microns in both eyes). The dilated fundus examination was similar to the previous color picture and did not disclose peripheral hemorrages recalling extended peripheral retinal ischemia. Humphrey Visual Field disclosed an altitudinal inferior scotoma and a peripheral inferior scotoma OR and was in the normal range OS, i.e. did not recall normal tension glaucoma OS . There were no papillary drusen on the autofluorescence picture, ON volume was increased (11.77 mm3 OR versus 5.75 OS) on SD-OCT (Heidelberg Engineering®) OR, Retinal Nerve Fiber (RNFL) and RGC layers thicknesses were normal Marked epimacular hypereflectivity OR with foveolar depression inversion, moderately increased total volume and central foveolar thickness (CFT) (428 microns versus 328 OS), and a whitish aspect of the supero-temporal internal retinal layers recalling ischemic edema, were present . EDI CFT was incresead at 315 microns (versus 273 microns OS), with focal pachyvessels on the video mapping . OCT-Angiography disclosed focal perfusion defects in both the retinal and chorio-capillaris circulations , and central alterations of the PR1 layer on en-face OCT

Altogether the clinical picture evoked a NAION with venous sub-occlusion, recalling Fraenkel’s et al early hypothesis of an ET interstitial diffusion-related venous vasoconstriction behind the lamina cribrosa (2), as much as a rupture of the BRB was present in the optic nerve area (hemorrage along the optic disc). Choroidal vascular drop-out was suggested by the severity and rapidity of the VF impairment (31). The extremely rapid development of a significant “epiretinal membrane”, that we interpreted as a reactive - and protective, in absence of cystoid macular edema (CME) - ET 2-induced astrocytic proliferation (reviewed in 32), was as an additional sign of severe ischemia.

The mention of the retro-orbital pain evoking a “ciliary angor”, the absence of any inflammatory syndrome and of the usual metabolic syndrome in the emergency blood test, oriented the etiology towards a FS. And indeed anamnesis collected many features of the FS, i.e. hypotension (“non dipper” profile with one symptomatic nocturnal episode of hypotension on the MAPA), migrains, hypersensitivity to cold, stress, noise, smells, and medicines, history of a spontaneously resolutive hydrops six months earlier, and of paroxystic episods of vertigo (which had driven a prior negative brain RMI investigation for Multiple Sclerosis, a frequent record among FS patients (33) and of paroxystic visual field alterations (7)(9), that were actually recorded several times along the follow-up.

The diagnosis of FS was eventually confirmed in the Ophthalmology Department in Basel University on April 10th, with elevated retinal venous pressure (20 to 25mmHg versus 10-15 OS) (4)(7)(9), reduced perfusion in the central retinal artery and veins on ocular Doppler (respectively 8.3 cm/second OR velocity versus 14.1 mmHg OS, and 3.1/second OR versus 5.9 cm OS), and impaired vasodilation upon flicker light-dependant shear stress on the Dynamic Vessel Analyser testing (7-9). In addition atherosclerotic plaques were absent on carotid Doppler.

On March 4th, the patient was at length informed about the FS, a possible off label rhEPO IVI, and a related written informed consent on the ratio risk-benefits was delivered.

By March 7th, she returned on an emergency basis because of vision worsening OR. VA was unchanged, intraocular pressure was at 13, but Visual Field showed a worsening of the central and inferior scotomas with a decreased foveolar threshold, from 33 to 29 decibels. SD-OCT showed a 10% increase in the CFT volume.

On the very same day, an off label rhEPO IVI OR (EPREX® 2000 units, 0,05 cc in a pre-filled syringe) was performed in the operating theater, i.e. the dose reported by Modarres et al (27), and twenty times inferior to the usual weekly intravenous dose for treatment of chronic anemia secondary to CKD. Intra venous acetazolamide (500 milligrams) was performed prior to the injection, to prevent any increase in intra-ocular pressure. The patient was discharged with a prescription of chlorydrate betaxolol (Betoptic® 0.5 %) two drops a day, and high dose daily magnesium supplementation (600 mgr).

Incidentally the patient developed bradycardia the day after, after altogether instillation of 4 drops of betaxolol only, that was replaced by acetazolamide drops, i.e. a typical hypersensitivity reaction to medications in the FS (7)(9).

Subjective vision improvement was recorded as early as D1 after injection. By March 18 th, eleven days post rhEPO IVI, BCVA was improved at 20/63, the altitudinal scotoma had resolved (Fig. 5), Posterior Vitreous Detachment had developed with a disturbing marked Weiss ring, optic disc swelling had decreased; vasculogenesis within the retinal plexi and some regression of PR1 alterations were visible on OCT-en face. Indeed by 11 days post EPO significant functional, neuronal and vascular rescue were observed, while the natural evolution had been seriously vision threatening.

However cystoid ME (CME) had developed . Indo Cyanin Green-Cine Video Angiography (ICG-CVA) OR, performed on March 23, i.e. 16 days after the rhEPO IVI, showed a persistent drop in ocular perfusion: ciliary and central retinal artery perfusion timings were dramatically delayed at respectively 21 and 25 seconds, central retinal vein perfusion initiated by 35 seconds, was pulsatile, and completed by 50 seconds only (video 3). Choroidal pachyveins matching the ones on SD-OCT video mapping were present in the temporal superior and inferior fields, and crossed the macula; capillary exclusion territories were present in the macula and around the optic disc.

By April 1, 23 days after the rhEPO injection, VA was unchanged, but CME and perfusion voids in the superficial deep capillary plexi and choriocapillaris were worsened, and optic disc swelling had recurred back to baseline, in a context of repeated episodes of systemic hypotension; and actually Nifepidin-Ratiopharm® oral drops (34), that had been delivered via a Temporary Use Authorization from the central Pharmacology Department in Assistance Publique Hopitaux de Paris, had had to be stopped because of hypersensitivity.

A second off label rhEPO IVI was performed in the same conditions on April 3, i.e. approximately one month after the first one.

Evolution was favourable as early as the day after EPO injection 2: VA was improved at 20/40, CME was reduced, and perfusion improved in the superficial retinal plexus as well as in the choriocapillaris. By week 4 after EPO injection 2, CME was much decreased, i.e. without anti VEGF injection. On august 19th, by week 18 after EPO 2, perfusion on ICG-CVA was greatly improved , with ciliary timing at 18 seconds, central retinal artery at 20 seconds and venous return from 23 to 36 seconds, still pulsatile. Capillary exclusion territories were visible in the macula and temporal to the macula after the capillary flood time that went on by 20.5 until 22.5 seconds (video 4); they were no longer persistent at intermediate and late timings.

Last complete follow-up was recorded on January 7, 2021, at 22 months from EPO injection 2. BCVA was at 20/40, ON volume had dropped at 7.46 mm3, a sequaelar superior deficit was present in the RNFL with some corresponding residual defects on the inferior para central Visual Field , CFT was at 384 mm3 with an epimacular hyperreflectivity without ME, EDI CFT was dropped at 230 microns. Perfusion on ICG-CVA was not normalized, but even more improved, with ciliary timing at 15 seconds, central retinal artery at 16 seconds and venous return from 22 to 31 seconds, still pulsatile , indicating that VP was still above IOP. OCT-A showed persisting perfusion voids, especially at the optic disc and within the deep retinal capillary plexus. The latter were present at some degree in the OS as well . Choriocapillaris and PR1 layer were dramatically improved.

Last recorded BCVA was at 20/32 by February 14, 2022, at 34 months from EPO 2. SD-OCT showed stable gliosis hypertrophy and mild alterations of the external layers .

Discussion

What was striking in the initial clinical phenotype of CRVO was the contrast between the moderate venous dilation, and the intensity of ischemia, that were illustrating the pioneer hypothesis of Professor Flammer‘s team regarding the pivotal role of ET in VO (2), recently confirmed (3)(35), i.e. the local venous constriction backwards the lamina cribrosa, induced by diffusion of ET-1 within the vascular interstitium, in reaction to hypoxia. NAION was actually the primary and prevailing alteration, and ocular hypoperfusion was confirmed via ICG-CVA, as well as by the ocular Doppler performed in Basel. ICG-CVA confirmed the choroidal drop-out suggested by the severity of the VF impairment (31) and by OCT-A in the choriocapillaris. Venous pressure measurement, which instrumentation is now available (8), should become part of routine eye examination in case of RVO, as it is key to guide cases analysis and personalized therapeutical options.

Indeed, the endogenous EPO pathway is the dominant one activated by hypoxia and is synergetic with the VEGF pathway, and coherently it is expressed along to VEGF in the vitreous in human RVO (36). Diseases develop when the individual limiting stress threshold for efficient adaptative reactive capacity gets overwhelmed. In this case by Week 3 after symtoms onset, neuronal and vascular resilience mechanisms were no longer operative, but the BRB, compromised at the ON, was still maintained in the retina.

As mentioned in the introduction, the scientific rationale for the use of EPO was well demonstrated by that time, as well as the capacities of exogenous EPO to mimic endogenous EPO vasculogenesis, neurogenesis and synaptogenesis, restoration of the balance between ET-1 and NO. Improvement of chorioretinal blood flow was actually illustrated by the evolution of the choriocapillaris perfusion on repeated OCT-A and ICG-CVA. The anti-apoptotic effect of EPO (16) seems as much appropriate in case of RVO as the caspase-9 activation is possibly another overlooked co-factor (6).

All the conditions for translation into off label clinical use were present: severe vision loss with daily worsening and unlikely spontaneous favourable evolution, absence of toxicity in the human pilot studies, of contradictory comorbidities and co-medications, and of context of intraocular neovascularization that might be exacerbated by EPO (37).

Why didn’t we treat the onset of CME by March 18th, i.e. eleven days after EPO IVI 1, by anti-VEGF therapy, the “standard-of-care” in CME for RVO ?

In addition to the context of functional, neuronal and vascular improvements obviated by rhEPO IVI by that timing in the present case, actually anti VEGF therapy does not address the underlying causative pathology. Coherently, anti-VEGF IVI : 1) may not be efficient in improving vision in RVO, despite its efficiency in resolving/improving CME (usually requiring repeated injections), as shown in the Retain study (56% of eyes with resolved ME continued to loose vision)(quoted in (1) 2) eventually may be followed by serum ET-1 levels increase and VA reduction (in 25% of cases in a series of twenty eyes with BRVO) (38) and by increased areas of non perfusion in OCT-A (39). Rather did we perform a second hrEPO IVI, and actually we consider open the question whether the perfusion improvement, that was progressive, might have been accelerated/improved via repeated rhEPO IVI, on a three to four weeks basis.

The development of CME itself, involving a breakdown of the BRB, i.e. of part of the complex retinal armentorium resilience to hypoxia, was somewhat paradoxical in the context of improvement after the first EPO injection, as EPO restores the BRB (24), and as much as it was suggested that EPO inhibits glial osmotic swelling, one cause of ME, via VEGF induction (40). Possible explanations were: 1) the vascular hyperpermeability induced by the up-regulation of VEGF gene expression via EPO (41) 2) the ongoing causative disease, of chronic nature, that was obviated by the ICG-CVA and the Basel investigation, responsible for overwhelming the gliosis-dependant capacity of resilience to hypoxia 3) a combination of both. I/R seemed excluded: EPO precisely mimics hypoxic reconditioning as shown in over ten years publications, including in the retina (20), and as EPO therapy is part of the current strategy for stabilization of the endothelial glycocalix against I/R injury (42-43). An additional and not exclusive possible explanation was the potential antagonist action of EPO on GFAP astrocytes proliferation, as mentioned in the introduction (18), that might have counteracted the reactive protective hypertrophic gliosis, still fully operative prior to EPO injection, and that was eventually restored during the follow-up, where epiretinal hyperreflectivity without ME and ongoing chronic ischemia do coincide (Fig. 6 and video 6), as much as it is unlikely that EPO’s effect would exceed one month (cf infra). Inhibition of gliosis by EPO IVI might have been also part of the mechanism of rescue of RGG, compromised by gliosis in hypoxic conditions (44). Whatever the complex balance initially reached, then overwhelmed after EPO IVI 1, the challenge was rapidly overcome by the second EPO IVI without anti-VEGF injection, likely because the former was powerful enough to restore the threshold limit for resilience to hypoxia, that seemed no longer reached again during the relapse-free follow-up. Of note, this “epiretinal membrane “, which association to good vision is a proof of concept of its protective effect, must not be removed surgically, as it would suppress one of the mecanisms of resilience to hypoxia.

To our best knowledge, ICG-CVA was never reported in FS; it allows real time evaluation of the ocular perfusion and illustration of the universal rheological laws that control choroidal blood flow as well. Pachyveins recall a “reverse” veno-arteriolar reflex in the choroidal circulation, that is NO and autonomous nervous system-dependant, and that we suggested to be an adaptative choroidal microcirculation process to hypoxia (45). Their persistence during follow-up accounts for a persisting state of chronic ischemia.

The optimal timing for reperfusion via rhEPO in a non resolved issue:

in the case reported by Luscan and Roche, rhEPO IVI was performed on the very same day of disease onset, where it induced complete recovery from VA reduced at counting fingers at 1 meter, within 48 hours. This clinical human finding is on line with a recent rodent stroke study that established the timings for non lethal versus lethal ischemia of the neural and vascular lineages, and the optimized ones for beneficial reperfusion: the acute phase - from Day 1 where endothelial and neural cells are still preserved, to Day 7 where proliferation of pericytes and Progenitor Stem Cells are obtainable - and the chronic stage, up to Day 56, where vasculogenesis, neurogenesis and functional recovery are still possible, but with uncertain efficiency (46). In our particular case, PR rescue after rhEPO IVI 1 indicated that Week 3 was still timely. RhEPO IVI efficacy was shown to last between one (restoration of the BRB) and four weeks (antiapoptotic effect) in diabetic rats (24). The relapse after Week 3 post IVI 1 might indicate that it might be approximately the interval to be followed, should repeated injections be necessary.

The bilateral chronic perfusion defects on OCT-A at last follow-up indicate that both eyes remain in a condition of chronic ischemia and I/R, where endogenous EPO provides efficient ischemic pre-conditioning, but is potentially susceptible to be challenged during episodes of acute hypoxia that overwhelm the resilience threshold.

Conclusion

The present case advocates for individualized medicine with careful recording of the medical history, investigation of the systemic context, and exploiting of the available retinal multimodal imaging for accurate analytical interpretation of retinal diseases and their complex pathophysiology. The Flammer Syndrome is unfortunately overlooked in case of RVO; it should be suspected clinically in case of absence of the usual vascular and metabolic context, and in case of elevated RVP. RhEPO therapy is able to restore the beneficial endogenous EPO ischemic pre-conditioning in eyes submitted to challenging acute hypoxia episodes in addition to chronic ischemic stress, as in the Flammer Syndrome and fluctuating ocular blood flow, when it becomes compromised by the overwhelming of the hypoxic stress resilience threshold. The latter physiopathological explanation illuminates the cases of RVO where anti-VEGF therapy proved functionally inefficient, and/or worsened retinal ischemia. RhEPO therapy might be applied to other chronic ischemia and I/R conditions, as non neo-vascular Age Macular Degeneration (AMD), and actually EPO was listed in 2020 among the nineteen promising molecules in AMD in a pooling of four thousands (47).

#off-label therapy #JCRMHS #anti-VEGF therapy #Erythropoietin #Journal of Clinical Case Reports Medical Images and Health Sciences impact factor.#Primary Vascular Dysfunction

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nursingscience · 2 years ago

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Medical Abbreviations on Pharmacy Prescriptions

Here are some common medical abbreviations you may see on pharmacy prescriptions:

qd - once a day

bid - twice a day

tid - three times a day

qid - four times a day

qh - every hour

prn - as needed

pc - after meals

ac - before meals

hs - at bedtime

po - by mouth

IV - intravenous

IM - intramuscular

subQ - subcutaneous

mL - milliliter

mg - milligram

g - gram

mcg - microgram

stat - immediately, right away

NPO - nothing by mouth

cap - capsule

tab - tablet

susp - suspension

sol - solution

amp - ampule

inj - injection

Rx - prescription

C - Celsius

F - Fahrenheit

BP - blood pressure

HR - heart rate

RR - respiratory rate

WBC - white blood cell

RBC - red blood cell

Hgb - hemoglobin

Hct - hematocrit

PT - prothrombin time

INR - international normalized ratio

BUN - blood urea nitrogen

Cr - creatinine

Ca - calcium

K - potassium

Na - sodium

Cl - chloride

Mg - magnesium

PO2 - partial pressure of oxygen

PCO2 - partial pressure of carbon dioxide

ABG - arterial blood gas

CBC - complete blood count

BMP - basic metabolic panel

CMP - comprehensive metabolic panel.

ECG - electrocardiogram

EEG - electroencephalogram

MRI - magnetic resonance imaging

CT - computed tomography

PET - positron emission tomography

CXR - chest x-ray

CTX - chemotherapy

NSAID - nonsteroidal anti-inflammatory drug

DMARD - disease-modifying antirheumatic drug

ACE - angiotensin-converting enzyme

ARB - angiotensin receptor blocker

SSRI - selective serotonin reuptake inhibitor

TCA - tricyclic antidepressant

ADHD - attention deficit hyperactivity disorder

COPD - chronic obstructive pulmonary disease

CAD - coronary artery disease

CHF - congestive heart failure

DVT - deep vein thrombosis

GI - gastrointestinal

UTI - urinary tract infection

OTC - over-the-counter

Rx - prescription

OD - right eye

OS - left eye

OU - both eyes.

TID - thrombosis in dementia

TDS - ter die sumendum (three times a day)

BOM - bilaterally otitis media (infection in both ears)

BT - body temperature

C&S - culture and sensitivity

D/C - discontinue or discharge

D/W - dextrose in water

ETOH - ethyl alcohol

FUO - fever of unknown origin

H&P - history and physical examination

I&D - incision and drainage

I&O - intake and output

KVO - keep vein open

N&V - nausea and vomiting

PERRLA - pupils equal, round, reactive to light and accommodation

PR - per rectum

QAM - every morning

QHS - every bedtime

QOD - every other day

S/P - status post (after)

TPN - total parenteral nutrition

UA - urinalysis

URI - upper respiratory infection

UTI - urinary tract infection

VO - verbal order.

XRT - radiation therapy

YOB - year of birth

BRBPR - bright red blood per rectum

CX - cervix

DVT - deep vein thrombosis

GB - gallbladder

GU - genitourinary

HCV - hepatitis C virus

HPI - history of present illness

ICP - intracranial pressure

IVP - intravenous pyelogram

LMP - last menstrual period

MRSA - methicillin-resistant Staphylococcus aureus

MVA - motor vehicle accident

NKA - no known allergies

PEG - percutaneous endoscopic gastrostomy

PRN - pro re nata (as needed)

ROS - review of systems

SOB - shortness of breath

TAH - total abdominal hysterectomy.

TIA - transient ischemic attack

Tx - treatment

UC - ulcerative colitis

URI - upper respiratory infection

VSD - ventricular septal defect

VTE - venous thromboembolism

XR - x-ray

w/c - wheelchair

XRT - radiation therapy

ASD - atrial septal defect

Bx - biopsy

CAD - coronary artery disease

CKD - chronic kidney disease

CPAP - continuous positive airway pressure

DKA - diabetic ketoacidosis

DNR - do not resuscitate

ED - emergency department

ESRD - end-stage renal disease

FFP - fresh frozen plasma

FSH - follicle-stimulating hormone.

GCS - Glasgow Coma Scale

Hct - hematocrit

Hgb - hemoglobin

ICU - intensive care unit

IV - intravenous

JVD - jugular venous distension

K - potassium

L - liter

MCH - mean corpuscular hemoglobin

MI - myocardial infarction

Na - sodium

NGT - nasogastric tube

NPO - nothing by mouth

OR - operating room

PCN - penicillin

PRBC - packed red blood cells

PTT - partial thromboplastin time

RBC - red blood cells

RT - respiratory therapy

SOA - short of air.

SCD - sequential compression device

SIRS - systemic inflammatory response syndrome

STAT - immediately

T - temperature

TPN - total parenteral nutrition

WBC - white blood cells

ABG - arterial blood gas

A fib - atrial fibrillation

BPH - benign prostatic hypertrophy

CBC - complete blood count

CO2 - carbon dioxide

COPD - chronic obstructive pulmonary disease

CPR - cardiopulmonary resuscitation

CT - computed tomography

CXR - chest x-ray

D5W - dextrose 5% in water

Dx - diagnosis

ECG or EKG - electrocardiogram

EEG - electroencephalogram

ETO - early termination of pregnancy.

FHR - fetal heart rate

GSW - gunshot wound

H&P - history and physical exam

HCG - human chorionic gonadotropin

I&D - incision and drainage

IBS - irritable bowel syndrome

ICP - intracranial pressure

IM - intramuscular

INR - international normalized ratio

IOP - intraocular pressure

LFT - liver function test

LOC - level of consciousness

LP - lumbar puncture

NG - nasogastric

OA - osteoarthritis

OCD - obsessive-compulsive disorder

OTC - over-the-counter

P - pulse

PCA - patient-controlled analgesia

PERRLA - pupils equal, round, reactive to light and accommodation.

PFT - pulmonary function test

PICC - peripherally inserted central catheter

PO - by mouth

PRN - as needed

PT - physical therapy

PT - prothrombin time

PTSD - post-traumatic stress disorder

PVC - premature ventricular contraction

QD - once a day

QID - four times a day

RA - rheumatoid arthritis

RICE - rest, ice, compression, elevation

RSI - rapid sequence intubation

RSV - respiratory syncytial virus

SBP - systolic blood pressure

SLE - systemic lupus erythematosus

SSRI - selective serotonin reuptake inhibitor

STAT - immediately

TB - tuberculosis

TIA - transient ischemic attack.

TID - three times a day

TKO - to keep open

TNTC - too numerous to count

TPN - total parenteral nutrition

URI - upper respiratory infection

UTI - urinary tract infection

V-fib - ventricular fibrillation

V-tach - ventricular tachycardia

VA - visual acuity

WNL - within normal limits

AED - automated external defibrillator

ARDS - acute respiratory distress syndrome

BID - twice a day

BP - blood pressure

BUN - blood urea nitrogen

CAD - coronary artery disease

CHF - congestive heart failure

CVA - cerebrovascular accident

D/C - discontinue

DKA - diabetic ketoacidosis.

DM - diabetes mellitus

DVT - deep vein thrombosis

EGD - esophagogastroduodenoscopy

ER - emergency room

F - Fahrenheit

Fx - fracture

GI - gastrointestinal

GTT - glucose tolerance test

HCT - hematocrit

Hgb - hemoglobin

HRT - hormone replacement therapy

ICP - intracranial pressure

IDDM - insulin-dependent diabetes mellitus

IBS - irritable bowel syndrome

IM - intramuscular

IV - intravenous

K - potassium

KVO - keep vein open

L&D - labor and delivery

LASIK - laser-assisted in situ keratomileusis.

ROM - range of motion

RT - radiation therapy

Rx - prescription

SCD - sequential compression device

SOB - shortness of breath

STD - sexually transmitted disease

TENS - transcutaneous electrical nerve stimulation

TIA - transient ischemic attack

TSH - thyroid-stimulating hormone

UA - urinalysis

US - ultrasound

UTI - urinary tract infection

VD - venereal disease

VF - ventricular fibrillation

VT - ventricular tachycardia

WBC - white blood cell

XRT - radiation therapy

XR - x-ray

Zn - zinc

Z-pak - azithromycin (antibiotic).

AAA - abdominal aortic aneurysm

ABG - arterial blood gas

ACS - acute coronary syndrome

ADL - activities of daily living

AED - automated external defibrillator

AIDS - acquired immunodeficiency syndrome

ALS - amyotrophic lateral sclerosis

AMA - against medical advice

AML - acute myeloid leukemia

APAP - acetaminophen

ARDS - acute respiratory distress syndrome

ASCVD - atherosclerotic cardiovascular disease

BPH - benign prostatic hyperplasia

BUN - blood urea nitrogen

CABG - coronary artery bypass graft

CBC - complete blood count

CHF - congestive heart failure

COPD - chronic obstructive pulmonary disease

CPAP - continuous positive airway pressure

CRF - chronic renal failure.

CT - computed tomography

CVA - cerebrovascular accident

D&C - dilation and curettage

DVT - deep vein thrombosis

ECG/EKG - electrocardiogram

EEG - electroencephalogram

ESRD - end-stage renal disease

FSH - follicle-stimulating hormone

GERD - gastroesophageal reflux disease

GFR - glomerular filtration rate

HbA1c - glycated hemoglobin

Hct - hematocrit

HIV - human immunodeficiency virus

HPV - human papillomavirus

HTN - hypertension

IBD - inflammatory bowel disease

IBS - irritable bowel syndrome

ICU - intensive care unit

IDDM - insulin-dependent diabetes mellitus

IM - intramuscular.

IV - intravenous

LFT - liver function test

MI - myocardial infarction

MRI - magnetic resonance imaging

MS - multiple sclerosis

NPO - nothing by mouth

NS - normal saline

OCD - obsessive-compulsive disorder

OSA - obstructive sleep apnea

PCOS - polycystic ovary syndrome

PMS - premenstrual syndrome

PPD - purified protein derivative

PSA - prostate-specific antigen

PT - prothrombin time

PTT - partial thromboplastin time

RA - rheumatoid arthritis

RBC - red blood cell

RSV - respiratory syncytial virus

SLE - systemic lupus erythematosus

TB - tuberculosis.

It is important to remember that medical abbreviations can vary based on location and specialty.

Healthcare professionals should use medical abbreviations with caution and only when they are familiar with their meanings.

Patients should always communicate any questions or concerns they have about their medications or medical care to their healthcare provider or pharmacist to ensure they receive safe and accurate medical care.

10 notes · View notes

mcatmemoranda · 2 years ago

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When to worry about thrombosis — Rarely, patients with thrombocytopenia are at risk for thrombosis rather than, or in addition to, bleeding. While most of the implicated disorders are rare, it is important to consider them because urgent treatment may be needed to prevent life-threatening thrombotic events.

Examples include the following:

●Heparin-induced thrombocytopenia – A small percentage of patients exposed to heparin (less than 5 percent) will develop heparin-induced thrombocytopenia (HIT) in which antibodies to a platelet factor 4 epitope induced by heparin can cause thrombocytopenia and platelet activation, leading to life-threatening venous and/or arterial thrombosis. This diagnosis should be considered in a patient recently exposed to heparin who develops thrombocytopenia, thrombosis, anaphylaxis, or skin reactions. Treatment involves immediate discontinuation of heparin and administration of a non-heparin anticoagulant (e.g., dabigatran or bivalirudin).

●Vaccine-induced immune thrombotic thrombocytopenia (VITT) – VITT is a rare syndrome that occurs after vaccination with coronavirus disease 2019 (COVID-19) adenoviral vector vaccines (AstraZeneca and Janssen [Johnson & Johnson]). It resembles spontaneous HIT in that there is no prior heparin exposure, and it is associated with life-threatening venous and/or arterial thrombosis. Individuals with thrombosis and/or thrombocytopenia should be evaluated for recent administration of a COVID-19 vaccine within the preceding 5 to 30 days, and for which specific type of vaccine they received.

●Antiphospholipid syndrome – The antiphospholipid syndrome (APS) can develop in individuals with systemic lupus erythematosus, other medical conditions (eg, infection, medications, cancer), or in individuals without an underlying condition. Patients may have venous and/or arterial thrombosis. Treatment involves anticoagulation or aspirin, and treatment of any underlying condition.

●Disseminated intravascular coagulation – Patients with disseminated intravascular coagulation (DIC) are at risk of bleeding or thrombosis, usually venous. DIC is commonly seen in acutely ill patients with sepsis or malignancy, but it can also be seen in a variety of other conditions.

●Thrombotic microangiopathy – Thrombotic microangiopathies (TMAs) such as thrombocytopenic purpura (TTP), hemolytic uremic syndrome (HUS), or drug-induced TMA (DITMA) are associated with small-vessel platelet-rich thrombi. These microthrombi can occur in any organ and can be life-threatening. Plasma exchange for TTP may be life-saving and should be initiated immediately when TTP is suspected.

●Paroxysmal nocturnal hemoglobinuria – Paroxysmal nocturnal hemoglobinuria (PNH) is a rare condition caused by loss of glycosyl phosphatidylinositol from cell membranes. Thrombosis (often involving unusual locations such as intraabdominal or cerebral veins) can occur, along with hemolytic anemia and/or bone marrow failure. Treatment depends on the degree of cytopenias and the presence of thrombosis.

●ITP with a concomitant thrombotic disorder – Certain conditions can occur in patients with ITP increasing their risk of thrombosis such as atrial fibrillation or recent or previous deep vein thrombosis. Management of anticoagulation in that population can be challenging; however, it is important to note that the low platelet count is not protective against thrombosis, and anticoagulation is often indicated.

Work up:

Peripheral blood smear — Review of the peripheral blood smear is used to exclude pseudothrombocytopenia (eg, falsely low platelet count due to platelet clumping) and to evaluate morphologic abnormalities of blood cells that could be useful in determining the cause of thrombocytopenia. As an example, giant platelets may suggest a congenital platelet disorder (eg, MYH-9-related disorders, Bernard Soulier syndrome [BSS]); these may be counted as red blood cells by some automated counters.

Pseudothrombocytopenia — The possibility of pseudothrombocytopenia (ie, falsely low platelet count) should be eliminated before any further evaluation is undertaken. Pseudothrombocytopenia can occur in a number of settings, all of which can be identified by review of the peripheral blood smear and/or repeating the CBC using a non-EDTA anticoagulant:

●Incompletely mixed or inadequately anticoagulated samples may form a clot that traps platelets in the collection tube and prevents them from being counted.

●In approximately 0.1 percent of individuals, exposure of patient samples to the EDTA anticoagulant in the collection tube can induce platelet clumps or platelet rosettes around white blood cells (WBCs). These may be counted by automated counters as leukocytes rather than platelets. The mechanism is "naturally occurring" platelet autoantibodies directed against a concealed epitope on platelet membrane glycoprotein (GP) IIb/IIIa that becomes exposed by EDTA-induced dissociation of GPIIb/IIIa [45-52].

If platelet clumping is observed, the platelet count is repeated using heparin or sodium citrate as an anticoagulant in the collection tube. If citrate is used, the platelet count should be corrected for dilution caused by the amount of citrate solution; no such correction is needed for heparin. Alternatively, fresh, non-anticoagulated blood can be pipetted directly into platelet-counting diluent fluid.

RBC and WBC abnormalities — Abnormal RBC and WBC morphologies may suggest a specific condition.

Examples include the following:

●Schistocytes suggest a microangiopathic process (eg, DIC, TTP, HUS, DITMA).

●Nucleated RBCs, and Howell-Jolly bodies, may be seen post-splenectomy or occasionally in patients with poor splenic function.

●Spherocytes suggest immune-mediated hemolytic anemia or hereditary spherocytosis.

●Leukoerythroblastic findings, teardrop cells, nucleated RBCs, or immature granulocytes suggest an infiltrative process in the bone marrow.

●Leukocytosis with a predominance of bands and/or toxic granulations suggests infection.

●Immature WBCs (eg, myeloblasts) or dysplastic WBCs suggest leukemia or myelodysplasia.

●Multi-lobed/hypersegmented neutrophils (ie, more than 5 lobes) suggest a megaloblastic process (eg, B12/folate/copper deficiency).

HIV and HCV testing — Thrombocytopenia has been identified as an important "indicator condition" for HIV infection. Thus, adults with new thrombocytopenia should have HIV testing if not done recently.

Thrombocytopenia may also be seen with hepatitis C virus (HCV) infection; testing is appropriate for adults with thrombocytopenia if not done recently. Other laboratory testing — Aside from the testing mentioned above (CBC, review of peripheral smear, HIV and HCV testing), no additional laboratory testing is absolutely required in a patient with isolated thrombocytopenia. However, additional testing may be warranted in patients with other findings.

Examples of findings that may trigger other laboratory testing include the following:

●Symptoms or findings of systemic autoimmune disorders (eg, systemic lupus erythematosus [SLE], anti-phospholipid syndrome [APS]) may prompt testing for anti-nuclear antibodies or anti-phospholipid antibodies, respectively. We do not test for these in patients with isolated thrombocytopenia and no signs or symptoms suggestive of SLE or APS.

●Findings of liver disease should prompt measurements of hepatic enzymes and possibly tests of liver synthetic function (eg, albumin, coagulation testing), depending on the severity of the liver disease.

●Thrombosis should prompt consideration of DIC, heparin-induced thrombocytopenia (HIT) and related syndromes, and APS. Depending on the site of thrombosis and other hematologic findings, paroxysmal nocturnal hemoglobinuria (PNH) may also be a consideration.

●Microangiopathic changes on the peripheral smear should prompt coagulation testing (eg, PT, aPTT, fibrinogen) and measurement of serum lactate dehydrogenase (LDH) and renal function to evaluate for DIC, TTP, or HUS; with subsequent evaluation based on the results.

ADDITIONAL EVALUATION

Hematologist referral/consultation — Referral to a hematologist is appropriate to confirm any new diagnosis of a thrombocytopenic condition or to determine the cause of any unexplained thrombocytopenia. The urgency of referral depends on the degree of thrombocytopenia and other abnormalities, and the stability of the findings.

In hospitalized patients, some conditions are medical emergencies that require immediate action. Immediate hematologist involvement in diagnosis and management is appropriate for the following:

●Suspected thrombotic thrombocytopenic purpura (TTP) or hemolytic uremic syndrome (HUS).

●Suspected heparin-induced thrombocytopenia (HIT).

●Suspected COVID-19 vaccine-induced immune thrombotic thrombocytopenia (VITT).

●Suspected hematologic malignancy (eg, acute leukemia), aplastic anemia, or other bone marrow failure syndrome.

The consulting hematologist can also assist in diagnosis and management of patients with severe thrombocytopenia (ie, platelet count less than 50,000/microL) who have serious bleeding or require an urgent invasive procedure, and in pregnant women with severe thrombocytopenia, regardless of the cause.

Bone marrow evaluation — Bone marrow evaluation (aspirate and biopsy) is not required in all patients with thrombocytopenia. However, it may be helpful in some patients if the cause of thrombocytopenia is unclear, or if a primary hematologic disorder is suspected. A possible exception may be a clinical picture consistent with a nutrient deficiency in which a bone marrow would only be needed if a deficiency could not be documented, or if the hematologic findings did not resolve upon nutrient repletion.

The following bone marrow findings may be helpful:

●Normal or increased numbers of megakaryocytes suggests that the thrombocytopenia is due, at least in part, to a condition associated with platelet destruction (eg, ITP, drug-induced immune thrombocytopenia).

●Decreased megakaryocyte numbers, along with overall decreased or absent cellularity (picture 18 and picture 19), is consistent with decreased bone marrow production of platelets, as in aplastic anemia.

●In rare cases, severe reduction or absence of megakaryocytes with no other abnormalities (also called acquired amegakaryocytic thrombocytopenia or acquired pure megakaryocytic aplasia) may occur. This finding is most often reported in patients with SLE, and is typically due to an autoantibody directed against the thrombopoietin receptor.

●Megaloblastic changes in the RBC and granulocytic series suggest a nutrient deficiency (eg, vitamin B12, folate, copper) (picture 20), while dysplastic changes suggest a myelodysplastic disorder (picture 21 and picture 22).

●Granulomata, increased reticulin or collagen fibrosis (picture 23 and picture 24), or infiltration with malignant cells (picture 25) establishes the diagnosis of bone marrow invasion, especially when a leukoerythroblastic blood picture is also present.

GENERAL MANAGEMENT PRINCIPLES

There are some general management principles that apply to all patients with thrombocytopenia regardless of the cause, and for which questions may arise before a diagnosis has been established.

●Activity restrictions – Patients who are otherwise healthy and have no manifestations of petechiae or purpura may not require activity restrictions.

Individual considerations apply to participation in certain activities. As an example, individuals with severe thrombocytopenia (less than 50,000/microL) generally should not participate in extreme athletics such as boxing, rugby, and martial arts. However, no restrictions are necessary for usual activities or low-impact exercise.

●Anticoagulant and anti-platelet medications – For anticoagulant and anti-platelet medications, the clinical indications and risks associated with discontinuation (eg, thrombosis) are balanced against the bleeding risk associated with the degree of thrombocytopenia and of continuing the anticoagulant and/or anti-platelet medication [7]. Input from the consulting specialist who prescribed the medication and/or the hematologist may be sought. A discussion of anticoagulation in adults with thrombocytopenia is presented separately.

It is also important to note that thrombocytopenia by itself does not protect against venous or arterial thrombosis, and appropriate use of thromboprophylaxis or anticoagulants should not be withheld from a patient with mild to moderate thrombocytopenia (eg, greater than 50,000/microL) if it is indicated (eg, postoperatively). For patients with more severe thrombocytopenia, decisions are made on a case-by-case basis regarding the risks of bleeding and benefits of anticoagulation.

●Over-the-counter remedies – Patients should be educated about which non-prescription remedies interfere with platelet function (eg, aspirin, nonsteroidal anti-inflammatory drugs, ginkgo biloba). In general, these agents are avoided unless there is a specific indication for which equivalent alternatives are lacking.

●Safe platelet count for invasive procedures – Most platelet count thresholds for invasive procedures are based on weak observational evidence at best. In general, procedures with a greater risk of bleeding are performed at higher platelet counts. While there is some flexibility in individual circumstances, anesthesiologists and surgeons performing these procedures will have the last word. A listing of general guidelines used for different procedures is presented separately.

Optimal methods for raising the platelet count in preparation for an invasive procedure depend on the underlying condition (eg, corticosteroids or intravenous immune globulin (IVIG) for presumptive ITP; platelet transfusion for myelodysplastic syndromes). These approaches are discussed in detail in separate topic reviews.

Individuals with impaired platelet function may require platelet transfusions despite adequate platelet counts, depending on the procedure. Attention should also be paid to correcting coagulation abnormalities if present.

●Emergency management of bleeding – Urgent management of critical bleeding in the setting of severe thrombocytopenia requires immediate platelet transfusion, regardless of the underlying cause.

#thrombocytopenia #low platelet count #low platelets #thrombocytopenia wu

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minimallyinvasive · 7 months ago

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Exploring Minimally Invasive Treatments for May-Thurner Syndrome

The exploration of minimally invasive treatments for May-Thurner Syndrome represents a significant advancement in vascular medicine. Procedures such as endovascular stenting, balloon angioplasty, and catheter-directed thrombolysis offer effective alternatives to traditional surgery, providing patients with safer options and quicker recovery. For more details, visit our website.

#deep vein thrombosis st augustine #superficial venous reflux disease symptoms #end stage renal disease treatment st augustine

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delarra-clinic1 · 8 days ago

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When To Seek Help: Signs You May Need A Vascular Treatment

The vascular system, often referred to as the circulatory system, plays a crucial role in maintaining the health and functionality of your body. This intricate network of arteries, veins, and capillaries ensures that oxygenated blood reaches every part of your body while carrying away waste products. Given its importance, even minor disruptions in the vascular system can lead to significant health complications. But how do you know when to seek professional help for vascular issues? This blog will explore the key signs that indicate you may need vascular treatment, helping you make informed decisions about your health.

Understanding Vascular Health

Before delving into the warning signs, it's essential to understand the basics of vascular health. A healthy vascular system supports proper blood circulation, which is fundamental for delivering nutrients and oxygen to tissues and organs. Over time, factors like aging, lifestyle choices, and genetic predispositions can negatively impact vascular health, leading to conditions such as:

Peripheral Artery Disease (PAD)

Deep Vein Thrombosis (DVT)

Varicose veins

Aneurysms

Carotid artery disease

These conditions can range from mild discomfort to life-threatening emergencies, highlighting the importance of timely intervention.

Key Signs You May Need Vascular Treatment

Recognizing the signs of vascular problems can help prevent severe complications. Below are the most common symptoms and conditions that warrant professional evaluation and potential treatment:

1. Persistent Leg Pain or Cramping

Leg pain, especially during physical activity, could be a sign of Peripheral Artery Disease (PAD). This condition occurs when narrowed arteries reduce blood flow to the limbs. The pain, often described as cramping or aching, typically subsides with rest but may return upon exertion.

2. Swelling in the Legs

Swelling in one or both legs can indicate venous insufficiency or Deep Vein Thrombosis (DVT). DVT is particularly concerning as it involves a blood clot that can travel to the lungs, causing a potentially fatal pulmonary embolism. Chronic swelling should always be evaluated by a healthcare provider.

3. Non-healing Wounds or Ulcers

Slow-healing or non-healing wounds, particularly on the legs or feet, could signal poor blood circulation due to PAD or diabetes-related vascular issues. These wounds are often accompanied by discoloration, pain, or infection and require prompt medical attention.

4. Visible Varicose Veins

Varicose veins are twisted, enlarged veins visible just under the surface of the skin. While they may seem primarily cosmetic, they can also cause discomfort, heaviness, or throbbing in the legs. Severe cases may require treatment to prevent complications like blood clots or ulcers.

5. Sudden Numbness or Weakness

Sudden numbness, weakness, or difficulty speaking could be signs of a transient ischemic attack (TIA) or stroke. These conditions are often linked to carotid artery disease, where plaque buildup restricts blood flow to the brain. Immediate medical intervention is critical.

6. Cold or Discolored Extremities

Experiencing cold, pale, or bluish fingers or toes may indicate poor blood flow due to arterial blockages. This symptom can also be associated with conditions like Raynaud's phenomenon or advanced PAD.

7. Family History of Vascular Disease

A family history of vascular conditions, such as aneurysms or blood clots, increases your risk. Regular check-ups and screenings are crucial if you have a genetic predisposition to vascular issues.

When to Seek Medical Attention

It’s essential to consult a healthcare provider if you experience any of the symptoms mentioned above. While some conditions may initially appear mild, they can quickly escalate if left untreated. Delarra Clinic specializes in diagnosing and treating vascular conditions, offering a range of advanced diagnostic tools such as Doppler ultrasound, CT angiography, and vascular lab tests.

Types of Vascular Treatments

Modern vascular treatments are highly advanced and minimally invasive, making recovery faster and more comfortable. Some common treatment options include:

1. Lifestyle Modifications

For mild vascular issues, doctors may recommend lifestyle changes such as:

Quitting smoking

Regular exercise

Healthy eating

Weight management

2. Medications

Medications can manage symptoms and reduce risks, including:

Blood thinners to prevent clots

Cholesterol-lowering drugs

Pain relievers for symptomatic relief

3. Minimally Invasive Procedures

Technological advancements have made treatments less invasive, such as:

Endovascular stent placement

Angioplasty

Laser treatments for varicose veins

4. Surgical Options

In severe cases, surgery may be necessary, including:

Bypass surgery to restore blood flow

Carotid endarterectomy to remove plaque

Aneurysm repair

Conclusion

Vascular health is fundamental to your overall well-being. Ignoring early warning signs can lead to severe complications, making it crucial to recognize and address symptoms promptly. Whether it’s persistent leg pain, swelling, or visible varicose veins, consulting a specialist can provide clarity and treatment options.

At Delarra Clinic, expert vascular care is within your reach. Don’t wait for symptoms to worsen—take proactive steps to ensure your circulatory health. Remember, early detection and timely treatment are the keys to maintaining a healthy vascular system and enhancing your quality of life.

Also, Read: 10 types of facial treatments that will restore your glow

#aesthetic treatments in denia #botox treatment in denia #advanced hair transplant

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healthpackageservicesatultrascan · 24 days ago

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Colour Doppler Test for Legs: Diagnosing Circulation Issues Effectively

Circulation problems in the legs can lead to severe health complications if left undiagnosed. The colour Doppler test for legs is a highly effective diagnostic tool that helps detect issues with blood flow, such as blockages, blood clots, or narrowing of blood vessels. It is a non-invasive procedure that uses sound waves to create an image of blood flow in the leg veins and arteries. If you're experiencing leg pain, swelling, or cramps, a colour Doppler test for legs can be a crucial step in identifying the underlying cause and preventing more serious conditions.

In this article, we will explore the importance of the colour Doppler test for legs, its procedure, and how it helps diagnose vascular issues. Additionally, we will discuss the availability and pricing of Doppler tests, particularly in Indore, at trusted centres like Ultrascan Diagnostics, which is known as the best diagnostic centre in Indore.

What is a Colour Doppler Test for Legs?

A colour Doppler test for legs is a specialized ultrasound technique that provides detailed images of the blood flow through the veins and arteries in the legs. The test uses high-frequency sound waves, which are reflected off moving blood cells. The reflections are then converted into images showing blood flow patterns, velocity, and direction.

Unlike traditional ultrasound, which shows static images, the colour Doppler test adds colour to the images, with different colours representing the direction of blood flow. This allows doctors to assess:

Blood clots (deep vein thrombosis)

Narrowing or blockages in blood vessels (arterial stenosis)

Venous insufficiency

Varicose veins

Peripheral artery disease (PAD)

By identifying these issues early, doctors can provide timely treatment to prevent further complications, such as stroke or heart attack.

When Should You Get a Colour Doppler Test for Legs?

If you experience any of the following symptoms, it may be time to consider a colour Doppler test for legs:

Leg pain or cramping that is persistent or worsens

Swelling in the legs, ankles, or feet

Visible varicose veins

Skin discolouration or ulcers on the legs

Numbness or tingling sensations in the legs or feet

A family history of vascular diseases or blood clotting disorders

A colour Doppler test is particularly important for individuals at risk of conditions like deep vein thrombosis (DVT), varicose veins, or peripheral artery disease (PAD). These conditions can result in serious complications if untreated, making early diagnosis crucial.

Benefits of the Colour Doppler Test for Legs

The colour Doppler test for legs offers several advantages in diagnosing circulation issues:

Non-invasive: No incisions or injections are required, making it a safe procedure.

Accurate Diagnosis: It provides real-time images of blood flow, helping detect issues like blockages or narrowing in the blood vessels.

Quick Results: The test is relatively fast, typically taking 20-30 minutes, and provides immediate results.

No Radiation: Unlike some imaging tests, colour Doppler ultrasound does not use harmful radiation, making it a safe choice for patients of all ages.

Monitoring Chronic Conditions: For patients with a history of vascular issues, regular Doppler tests can help monitor changes in blood flow and vascular health.

Understanding the Colour Doppler Test Price

One of the concerns patients often have when considering diagnostic tests is the colour Doppler test price. The cost of a colour Doppler ultrasound can vary based on factors like location, diagnostic centre, and the complexity of the test. However, at Ultrascan Diagnostics, one of the best diagnostic centres in Indore, we strive to offer competitive pricing for all Doppler tests, including the colour Doppler test for legs.

If you are concerned about the colour Doppler ultrasound price, our team will provide you with a clear breakdown of the costs, ensuring that you understand the pricing structure before proceeding with the test. We also offer additional services like renal Doppler tests, carotid Doppler tests, and penile Doppler tests.

How to Prepare for a Colour Doppler Test for Legs?

Preparing for a colour Doppler test for legs is simple and requires no special steps. However, your doctor might recommend the following:

Avoid wearing tight clothing around your legs to allow easier access for the ultrasound probe.

Stay hydrated before the test, as having a well-hydrated body can improve the quality of the test images.

There is typically no need for fasting, and you can resume normal activities immediately after the test.

Why Choose Ultrascan Diagnostics for Your Doppler Test?

At Ultrascan Diagnostics, we offer top-tier diagnostic services in Indore. Our colour Doppler test for legs is conducted using the latest ultrasound technology, ensuring precise and reliable results. We also offer:

Affordable pricing: Transparent and competitive doppler scan prices, with no hidden fees.

Experienced medical professionals: Our skilled technicians and radiologists ensure accurate testing and interpretation of results.

Convenient location: Centrally located in Indore, making it easy for you to access our services.

Comprehensive diagnostic options: From renal Doppler tests to fetal Doppler scans, we offer a wide range of diagnostic services.

Frequently Asked Questions (FAQs)

1. What is the purpose of a colour Doppler test for legs?

A colour Doppler test for legs is used to assess blood flow through the veins and arteries in the legs. It helps diagnose conditions such as varicose veins, blood clots, peripheral artery disease, and venous insufficiency.

2. How long does the colour Doppler test for legs take?

The colour Doppler test for legs usually takes between 20 and 30 minutes. It is a quick and non-invasive procedure that provides immediate results.

3. Are there any risks associated with the colour Doppler test for legs?

No, the colour Doppler test for legs is entirely safe and non-invasive. It uses high-frequency sound waves and does not involve radiation, making it suitable for patients of all ages.

Conclusion

The colour Doppler test for legs is a vital diagnostic tool for identifying circulation problems and vascular issues in the legs. Whether you're experiencing symptoms like leg pain, swelling, or visible varicose veins, this test can help determine the underlying cause and guide appropriate treatment. Early detection of circulation issues can prevent severe complications like strokes or amputations, making regular check-ups essential.

If you're looking for a reliable and affordable Doppler test near me or need a colour Doppler test for legs, visit Ultrascan Diagnostics in Indore, the best diagnostic centre in Indore. We offer comprehensive diagnostic services with advanced technology, skilled professionals, and competitive pricing. Schedule your appointment today and take the first step towards maintaining your vascular health! Are you experiencing leg pain or swelling? Contact us for more information on Doppler test prices, or book your appointment online now! Let us help you maintain your health with our expert diagnostic services.

#diagnostic ultrasound #diagnosticprocess

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